about
The genetic and genomic background of multiple myeloma patients achieving complete response after induction therapy with bortezomib, thalidomide and dexamethasone (VTD)Therapeutic targeting of hypoxia and hypoxia-inducible factor 1 alpha in multiple myeloma.Opposite activation of the Hedgehog pathway in CD138+ plasma cells and CD138-CD19+ B cells identifies two subgroups of patients with multiple myeloma and different prognosis.HIF-1α inhibition blocks the cross talk between multiple myeloma plasma cells and tumor microenvironment.Hypoxia inducible factor-1 alpha as a therapeutic target in multiple myeloma.Chibby drives β catenin cytoplasmic accumulation leading to activation of the unfolded protein response in BCR-ABL1+ cells.Cytoplasmatic compartmentalization by Bcr-Abl promotes TET2 loss-of-function in chronic myeloid leukemia.Cap dependent translation contributes to resistance of myeloma cells to bortezomib.PET/CT Improves the Definition of Complete Response and Allows to Detect Otherwise Unidentifiable Skeletal Progression in Multiple Myeloma.Analysis of mismatch repair gene mutations in Turkish HNPCC patients.Bortezomib-based therapy combined with high cut-off hemodialysis is highly effective in newly diagnosed multiple myeloma patients with severe renal impairment.Gadd45a transcriptional induction elicited by the Aurora kinase inhibitor MK-0457 in Bcr-Abl-expressing cells is driven by Oct-1 transcription factor.Relative role of APC and MUTYH mutations in the pathogenesis of familial adenomatous polyposis.
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0000-0003-3314-0037